scholarly journals Estrogenic G protein-coupled receptor 30 signaling is involved in regulation of endometrial carcinoma by promoting proliferation, invasion potential, and interleukin-6 secretion via the MEK/ERK mitogen-activated protein kinase pathway

2009 ◽  
Vol 100 (6) ◽  
pp. 1051-1061 ◽  
Author(s):  
Yin-Yan He ◽  
Bin Cai ◽  
Yi-Xia Yang ◽  
Xue-Lian Liu ◽  
Xiao-Ping Wan
Keyword(s):  
Protein Kinase ◽  
Endometrial Carcinoma ◽  
G Protein ◽  
Interleukin 6 ◽  
Mitogen Activated Protein Kinase ◽  
G Protein Coupled Receptor ◽  
Invasion Potential ◽  
Mitogen Activated Protein ◽  
G Protein Coupled ◽  
Kinase Pathway

scholarly journals Essential Role for G Protein-coupled Receptor Endocytosis in the Activation of Mitogen-activated Protein Kinase

1998 ◽  
Vol 273 (2) ◽  
pp. 685-688 ◽  
Author(s):  
Yehia Daaka ◽  
Louis M. Luttrell ◽  
Seungkirl Ahn ◽  
Gregory J. Della Rocca ◽  
Stephen S. G. Ferguson ◽  
...  
Keyword(s):  
Protein Kinase ◽  
G Protein ◽  
Essential Role ◽  
Mitogen Activated Protein Kinase ◽  
G Protein Coupled Receptor ◽  
Receptor Endocytosis ◽  
Mitogen Activated Protein ◽  
G Protein Coupled

scholarly journals G Protein-Coupled Receptor-Mediated Mitogen-Activated Protein Kinase Activation through Cooperation of Gαq and Gαi Signals

2000 ◽  
Vol 20 (18) ◽  
pp. 6837-6848 ◽  
Author(s):  
Andree Blaukat ◽  
Ana Barac ◽  
Michael J. Cross ◽  
Stefan Offermanns ◽  
Ivan Dikic
Keyword(s):  
Protein Kinase ◽  
G Protein ◽  
Tyrosine Kinases ◽  
Synergistic Effects ◽  
Mitogen Activated Protein Kinase ◽  
General Mechanism ◽  
Mitogen Activated Protein ◽  
Novel Concept ◽  
G Protein Coupled ◽  
Stimulation Of

ABSTRACT G protein-coupled receptors (GPCRs) have been shown to stimulate extracellular regulated kinases (ERKs) through a number of linear pathways that are initiated by Gq/11 or Giproteins. We studied signaling to the ERK cascade by receptors that simultaneously activate both G protein subfamilies. In HEK293T cells, bradykinin B2 receptor (B2R)-induced stimulation of ERK2 and transcriptional activity of Elk1 are dependent on Gαq-mediated protein kinase C (PKC) and on Gαi-induced Ras activation, while they are independent of Gβγ subunits, phosphatidylinositol 3-kinase, and tyrosine kinases. Similar results were obtained with m1 and m3muscarinic receptors in HEK293T cells and with the B2R in human and mouse fibroblasts, indicating a general mechanism in signaling toward the ERK cascade. Furthermore, the bradykinin-induced activation of ERK is strongly reduced in Gαq/11-deficient fibroblasts. In addition, we found that constitutively active mutants of Gαq/11 or Gαi proteins alone poorly stimulate ERK2, whereas a combination of both led to synergistic effects. We conclude that dually coupled GPCRs require a cooperation of Gαi- and Gq/11-mediated pathways for efficient stimulation of the ERK cascade. Cooperative signaling by multiple G proteins thus might represent a novel concept implicated in the regulation of cellular responses by GPCRs.

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